Changes In Systemic Vascular Resistance Index Research Articles

Hemodynamic Changes During Surgical Decompression in Traumatic Brain Injury Patients

To understand the hemodynamic changes that occur with surgical decompression of lesions caused by traumatic brain injury. In this prospective, observational study, patients with traumatic brain injury requiring craniotomy within 48 hours of injury were recruited. Cardiac index (CI), stroke volume index, stroke volume variation, systemic vascular resistance index (SVRI), heart rate, and mean arterial pressure were monitored throughout surgery using a FloTrac transducer. Standard anesthetic and surgical regimens were followed. Hemodynamic data in 107 patients were compared before skin incision and after hematoma decompression (comparable anesthetic state). There was a significant increase in CI and stroke volume index and a decrease in SVRI and mean arterial pressure following surgical decompression. On subgroup analysis based on preincision CI, the changes were similar in patients with low and normal CI, whereas in patients with high CI, SVRI did not decrease significantly. High preincision CI with no change in SVRI with decompression was associated with poor neurologic outcome at discharge. In patients with TBI, surgical decompression leads to an increase in CI and a decrease in mean arterial pressure owing to a decrease in SVRI in patients with preincision low or normal cardiac output. These changes were not seen in patients with preincision high CI, and such patients had a poor neurologic outcome.

Intravenous Flurbiprofen Axetil Can Stabilize the Hemodynamic Instability Due to Mesenteric Traction Syndrome—Evaluation With Continuous Measurement of the Systemic Vascular Resistance Index Using a FloTrac® Sensor

Evaluation of the stabilizing effect of intravenous flurbiprofen axetil against hemodynamic instability due to mesenteric traction syndrome (MTS) by continuous measurement of systemic vascular resistance index (SVRI) using a FloTrac(®) sensor was evaluated. Prospective randomized trial. A single-center study performed in an educational hospital. Two prospective studies were carried out, each with 40 patients scheduled for elective open abdominal surgery. Twenty patients received 50 mg of flurbiprofen axetil after the recognition of MTS by the anesthesiologist (group FT). The remaining patients served as controls (groups CP and CT). SVRI data was collected every 20 seconds for 1 hour after starting the laparotomy. The average SVRI prior to skin incision was taken as the baseline. Following 3 values were devised to evaluate MTS: the S-value (sum total of changes in SVRI from baseline), the T-value (period during which SVRI remained 20% or more below baseline), and the M-value (maximum change in SVRI from baseline). In group FP, decrease in SVRI was smaller than in group CP, and statistical differences in the 3 values were found. In group FT, SVRI recovered earlier than in group CT, and statistical differences were found in S-value and T-value. However, the M-value had no statistical differences. Intravenous flurbiprofen axetil can stabilize the hemodynamic instability due to MTS.

The influence of positive end-expiratory pressure on stroke volume variation for the accuracy of evaluating volume

To investigate the influence of positive end-expiratory pressure (PEEP) on hemodynamic and the ability of stroke volume variation (SVV) to predict cardiac preload. Thirty healthy anesthetized pigs were given tracheal intubation and ventilated. With the envelope method, they were all randomly divided into control group(n = 10), hypovolemia group (n = 10) and hypervolemia group (n = 10). Hypovolemia group were exsanguinated 20% blood volume within 5 minutes, hypervolemia group: additional infusion of hydroxyethyl starch equal to 20% blood volume,and control group: no intervention. In each group, ventilator settings were changed in a randomized order by changing PEEP [0, 5, 10 and 15 cm H(2)O, PEEP0, PEEP5, PEEP10, PEEP15, 1 cm H(2)O = 0.098 kPa]. The changes in hemodynamic parameters, including heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), cardiac index (CI), stroke volume index (SVI), systemic vascular resistance index (SVRI), intrathoracic blood volume index (ITBVI) and SVV, were monitored with a pulse-indicated continuous cardiac output (PiCCO). In the control group, HR, CVP, SVRI and SVV were evaluated accompanying with the increasing of PEEP, but CI, SVI and ITBVI submitted decreasing tendency. The value reached peaking or valley on the level of PEEP15, and there was significance compared with PEEP0 [HR (bpm): 124 ± 18 vs. 88 ± 12, CVP (mm Hg, 1 mm Hg = 0.133 kPa): 11 ± 1 vs. 8 ± 3, SVRI [kPa×s×L(-1)×m(-2)]: 289.6 ± 81.5 vs. 215.0 ± 79.1, SVV: (23 ± 6)% vs. (11 ± 2)%, CI [L×min(-1)×m(-2)]: 3.1 ± 0.8 vs. 4.3 ± 1.4, SVI [ml×min(-1)×m(-2)]: 26 ± 7 vs. 41 ± 4, ITBVI [ml/m(2)]: 440 ± 43 vs. 491 ± 47, all P < 0.05]. There was no change in MAP. In the hypovolemia group, HR, CVP and SVV were evaluated accompanying with the increasing of PEEP, but MAP, CI, SVI and ITBVI submitted decreasing tendency. The value reached peaking or valley on the level of PEEP15, and there was significance compared with PEEP0 [HR (bpm): 146 ± 31 vs. 115 ± 27, CVP (mm Hg): 11 ± 2 vs. 5 ± 1, SVV: (28 ± 4)% vs. (20 ± 5)%, MAP(mm Hg): 90 ± 26 vs. 115 ± 19, CI [L×min(-1)×m(-2)]: 2.3 ± 0.6 vs. 3.4 ± 1.1, SVI [ml×min(-1)×m(-2)]: 20 ± 6 vs. 31 ± 9, ITBVI [ml/m(2)]: 355 ± 34 vs. 396 ± 53, all P < 0.05]. There was no change in SVRI. In the hypervolemia group, SVV submitted increasing tendency with the increasing of PEEP, but CI, SVI and ITBVI were in the tendency of decreasing, the value reached peaking or valley on the level of PEEP15, and there was significance compared with PEEP0 [SVV: (18 ± 4)% vs. (6 ± 2)%, CI [L×min(-1)×m(-2)]: 4.5 ± 0.9 vs. 5.0 ± 1.2, SVI [ml×min(-1)×m(-2)]: 37 ± 9 vs. 49 ± 7, ITBVI [ml/m(2)]: 473 ± 71 vs. 565 ± 94, all P < 0.05]. There was no change in HR, MAP, CVP and SVRI. SVV was increased in the hypovolemia group compared with control group, and decreased in the hypervolemia group. In the control group, SVV was negatively related to CI on different level of PEEP [r(PEEP0) = -0.831, r(PEEP5) = -0.790, r(PEEP10) = -0.875, r(PEEP15) = -0.560, P < 0.05 or P < 0.01]. SVV was a precise indicator of cardiac preload, however high PEEP may influence hemodynamic and the accuracy of SVV.

Changes in blood pressure and systemic vascular resistance do not predict microvascular structure during treatment of mild essential hypertension

Essential hypertension is characterized by small artery remodeling and increased systemic vascular resistance (SVR). We hypothesized that changes in SVR index (SVRI) were associated with measures of small artery structure as reflected by minimum coronary and forearm vascular resistance (C-Rmin and F-Rmin, respectively). Also, we investigated how F-Rmin is related to C-Rmin, coronary flow reserve (CFR), left ventricular mass index (LVMI) and blood pressure (BP). Sixty-six never-treated patients with uncomplicated mild essential hypertension had the following measured at baseline: 24-h blood BP, LVMI, CFR and C-Rmin (echocardiography), F-Rmin (forearm plethysmography) and SVRI determined by a gas re-breathing method. After 6 months of antihypertensive therapy administered by the general practitioner, the patients returned for follow-up measurements. Changes in SVRI did not correlate to changes in F-Rmin (r = 0.001, P = 0.98) or C-Rmin (r = 0.13, P = 0.39) but did correlate to changes in CFR (r = 0.30, P = 0.04). Further analysis was performed by assigning the patients into two groups according to the median of drop in F-Rmin. When adjusted in a multivariate model, changes in F-Rmin (-8.1 ± 3.2%) were significantly associated with changes in C-Rmin (-9.3 ± 4.9%) and LVMI (-6.9 ± 1.7%) (P < 0.01), but not to either 24-h BP, SVRI or CFR. The results show that changes in neither BP nor SVRI reflected changes in minimum vascular resistance. However, changes in the forearm and coronary microcirculation occurred in parallel. Moreover, we demonstrated that neither BP nor SVRI reduction can predict changes in microvascular structure in hypertension. Thus, direct measurements of microvascular structure are needed to determine whether improvement is obtained.

Hemodynamic Monitoring during Erythrocytapheresis in Sickle Cell Disease Patients Using Impedance Cardiography

BACKGROUND: Erythrocytapheresis procedures are increasingly used in the treatment of severe acute complications of sickle cell disease (SCD). Some patients who undergo erythrocytapheresis experience dizziness during or after the procedure. There is no data in literature for hemodynamic monitoring of cardiac index (CI) and systemic vascular resistance index (SVRI) during erythrocytapheresis. We have previously shown that impedance cardiography (ICG) and invasive measures of CI by thermodilution techniques are significantly correlated in children.OBJECTIVES: We wanted to evaluate changes in CI and SVRI using ICG and to correlate these with systolic blood pressure (SBP) measurements in SCD patients while undergoing erythrocytapheresis.METHODS: Thirty one SCD patients who had 70 consecutive erythrocytapheresis procedures were included in this IRB approved study. ICG measurements (CI, SVRI, and blood pressure) were taken pre-erythrocytapheresis, 30 minutes after initiation of the procedure, one hour into erythrocytapheresis, and at the end of the procedure. ICG measurements were repeated in symptomatic patients before and after intervention with fluid administration.RESULTS: We evaluated hemodynamic data on 31 SCD patients, average age 12.8±5.2 years and 56% are female. SBP decreased below the base line during 33 procedures and increased above the baseline during 37 procedures. Among patients who had a decrease in SBP, 28/33 (84%) had decreased CI. Among them 22/28 (78%) had increased SVRI. Among patients who had an increase in SBP, 5/37 (14%) had increased CI. Among them 4/5 (80%) also had increased SVRI. Using paired t test, the changes in CI (P <0.001) and SVRI (P=0.0002) comparing to baseline are statistically significant. CI is negatively correlated with change in SVRI (Pearson correlation coefficient −0.8).CONCLUSIONS:In summary, the hemodynamic changes during erythrocytapheresis are probably multifactorial in origin and may include a combination of SVRI and CI changes. Confirmation of these findings may allow early intervention in some patients and minimize the risk of developing overt clinical symptoms during erythrocytapheresis.

Changes of ghrelin and brain natriuretic peptide levels in systemic vascular resistance after cardiopulmonary bypass

The application of cardiopulmonary bypass (CPB) using a heart-lung machine in open heart surgery is associated with numerous pathophysiological changes in the vascular system and the neurohormonal environment. In this study our purpose was to investigate whether the hormones brain natriuretic peptide (BNP) and ghrelin are involved in changes in the systemic vascular resistance index (SVRI) after CPB, using data from 20 patients who had undergone coronary artery bypass grafting accompanied by CPB. Hemodynamic measurements were obtained using a thermodilution catheter and included cardiac index and systemic vascular resistance index. Blood samples were taken before CPB, after CPB, and at 0 and 24 h postoperatively. The blood levels of total and acylated ghrelin were quantified by radioimmunoassay. Blood levels of BNP were measured by a fluorescence immunoassay kit. The SVRI was significantly higher at the end of CPB and at 0 h postoperatively than before CPB (end of CPB: 4282 +/- 1035 dyne x s x cm(-5) x m(-2), 0 h postoperatively: 3239 +/- 635 dyne x s x cm(-5) x m(-2) vs. before CPB: 2289 +/- 330 dyne x s x cm(-5) x m(-2), p < 0.05). Total and acylated ghrelin levels decreased until 0 h postoperatively but the change was not statistically significant. However, at 24 h after surgery, they showed a statistically significant increase over the initial ghrelin values (total before CPB: 1413.71 +/- 287.93 pg/ml vs. 24 h postoperatively: 1736.85 +/- 236.89 pg/ml; acylated ghrelin before CPB: 55.85 +/- 25.53 pg/ml vs. 24 h postoperatively: 106.28 +/- 30.86 pg/ml; p <0.05 for both). BNP values were markedly lower after than before CPB (before CPB: 69.07 +/- 48 pg/ml vs. after CPB: 21.96 +/- 13 pg/ml, p < 0.05) and reached a maximum value 24 h postoperatively (before CPB: 56.3 +/- 42 vs. after CPB: 454.7 +/- 229 pg/ml, p < 0.05). There was a weak negative correlation between the changes in SVRI and total and acylated ghrelin levels after the CPB period, but this was not statistically significant. However, there was a statistically significant negative correlation between SVRI and BNP after CPB and at 24 h postoperatively (r:-0.709, p < 0.01 and r:-0.649, p < 0.03, respectively). Taken together, our results show that the observed initial increases in ghrelin and/or BNP in the postoperative period (at 24 h) might be causally related to the decrease in the SVRI in the same period. However, further investigations are needed to clarify the significance of this observation with respect to that of SVRI.

Systolic blood pressure does not reliably identify vasoactive status in chronic heart failure

In chronic heart failure (CHF), titration of vasodilating medications is often guided by monitoring of systolic blood pressure (BP). However, systolic BP may not indicate the patient's true vasoactive status-best approximated by systemic vascular resistance-because cardiac output is also a contributing factor. Impedance cardiography (ICG) is a validated noninvasive method of measuring cardiac output and systemic vascular resistance. To evaluate the relationship between systolic BP and systemic vascular resistance index (SVRI) in patients with CHF, we retrospectively evaluated the systolic BP and SVRI from 71 consecutive patients during 615 CHF clinic visits. Measurement of systolic BP was through the oscillometric method and SVRI through ICG (BioZ ICG Monitor, CardioDynamics, San Diego, CA). Absolute values and relative changes in systolic BP and SVRI were compared and characterized by systolic BP grouping. The 71 patients were an average of 69.3 +/- 12.2 years, New York Heart Association functional class 2.52 +/- 0.6, 46.5% men, and 47.8% ischemic etiology. Frequency by systolic BP grouping was: <100 mm Hg in 67 subjects (10.9%), 100 to 119 mm Hg in 245 subjects (39.8%), and >/=120 mm Hg in 303 subjects (49.3%). The correlation (R(2) value) of systolic BP to SVRI was 0.21 (N = 615), and change in systolic BP to change in SVRI from previous visit was 0.27 (N = 547). In 138 visits in which systolic BP did not change by 5 mm Hg or more, SVRI changed by 20% or more in 41 (29.7%). In the 67 visits in which systolic BP was below 100, only 6 (9.0%) had low SVRI and 57 (85.1%) had normal SVRI. In the 245 visits with systolic BP 100 to 119, 58 (23.7%) had high SVRI. Measurement of systolic BP alone does not reliably indicate the degree of vasoconstriction or vasodilation that exists in patients with CHF. Measurement of SVRI by ICG may help guide determination of need and tolerance for vasodilating medications in CHF.

Cardiovascular responses to repetitive defibrillation during implantable cardioverter-defibrillator testing

Objective: To study the effects of electrical applications and subsequent postshock hypotension on myocardial performance and vascular tone during implantable cardioverter-defibrillator (ICD) placement. Design: Prospective, blinded, observational investigation. Setting: Single, university-affiliated institution. Participants: Twenty patients undergoing elective ICD placement and testing under general anesthesia. Interventions: None. Measurements and Main Results: Serial measurements were made of hemodynamic variables, left ventricular end-systolic (ESA) and end-diastolic (EDA) areas, fractional-area-of-contraction (FAC), time of hypoperfusion (when mean arterial pressure ≤50 mmHg postshock), and applied conversion energy. Multiple linear regression was performed to determine correlations among collected variables, and repeated measures analysis of variance was used to compare mean values. Minimal changes were detected in mean values of arterial, pulmonary, and central venous pressures; cardiac output; heart rate; and mixed venous saturation during repeated testing. Percentage changes in cardiac index (CI) rose and systemic vascular resistance index (SVRI) fell, however, as the number of shocks increased, reaching significance at the seventh and eighth shocks (v baseline; both p = 0.015). The percentage change in CI was linearly related to hypoperfusion time and accumulated energy (%ΔCI = 1.553 + [0.068 · Σ hypoperfusion time {sec}], r = 0.92, p < 0.001; %ΔCI = 0.326 + [0.125 · Σ Energy {J}], r = 0.94, p < 0.001). The percentage change in SVRI was inversely related to hypoperfusion time and accumulated energy (%ΔSVRI = 2.195 − [0.122 · Σ energy {J}], r = 0.79, p = 0.004; %ΔSVRI = 0.542 − [0.0634 − Σ hypoperfusion time {sec}], r = 0.73, p = 0.01). Echocardiographic EDA, ESA, and FAC were not significantly changed but showed substantial variability. Conclusion: Hemodynamic stability was generally well maintained during ICD placement and testing. Increases in CI were associated with concurrent reductions in systemic afterload, rather than enhanced FAC. Increasing postshock hypotension and applied energy were associated with decreases in CI and systemic afterload. Insignificant, but highly variable, changes were noted echocardiographically.

Effects of sevoflurane and isoflurane on systemic vascular resistance: use of cardiopulmonary bypass as a study model

We have examined the dose-related effects of sevoflurane and isoflurane on systemic vascular resistance (SVR) during cardiopulmonary bypass (CPB) in patients undergoing elective coronary artery surgery. Fifty-two patients were allocated randomly to one of six groups to receive 1.0, 2.0 or 3.0 vol% (inspiratory) sevoflurane or 0.6, 1.2 or 1.8 vol% isoflurane, or to a control group. During hypothermic (32-33 degrees C) non-pulsatile CPB, systemic vascular resistance index (SVRI) was recorded before administration of volatile anaesthetics and every 5 min for 20 min. Sevoflurane and isoflurane concentrations were measured next to the gas inlet port and at the gas outlet port of the oxygenator. Wash-in of sevoflurane occurred more rapidly than that of isoflurane, reaching a relatively steady state for both agents from the 10th to the 20th min. There was no significant change in SVRI in patients receiving 1.0 and 2.0 vol% sevoflurane, and 0.6 and 1.2 vol% isoflurane, compared with baseline values. However, 3 vol% sevoflurane decreased SVRI at 10, 15 and 20 min, and 1.8 vol% isoflurane decreased SVRI significantly at 15 and 20 min, whereas SVRI increased at 15 and 20 min in the control group. Thus during CPB, sevoflurane had similar vasodilator effects on SVRI as isoflurane.

The influence of isoflurane on the vascular reflex response to lung inflation in dogs.

Positive pressure ventilation can affect hemodynamic stability by neuroreflex-mediated activity. Inhalational anesthesia is known to attenuate the arterial baroreflex function; however, little information is known about the effect of volatile anesthetics on the lung inflation reflex. The influence of isoflurane on static lung inflation reflex-induced changes in venous capacitance and systemic resistance was investigated in dogs. After controlling carotid sinus pressure at 50 mmHg and initiating total cardiopulmonary bypass, the lungs were inflated to tracheal pressures of 10 and 20 mmHg. The systemic vascular resistance index (SVRI) decreased by 0.04 +/- 0.03 and 0.13 +/- 0.03 mmHg.kg.min.ml-1 during tracheal inflation pressures of 10 and 20 mmHg, respectively. There as an accompanying change in systemic vascular capacitance index (SVCI) by 1.0 +/- 0.65 and 3.3 +/- 0.82 ml.kg-1 during tracheal inflation pressures of 10 and 20 mmHg. The addition of isoflurane decreased the reflex vascular response to lung inflation in a dose-dependent manner. A concentration of 1 MAC isoflurane administered via the cardiopulmonary bypass machine attenuated the change in SVRI to tracheal inflation pressures of 10 and 20 mmHg by 75% and 67%, respectively. Isoflurane at 1 MAC also reduced the reflex capacitance response to tracheal pressures of 10 and 20 mmHg by 36% each. Lung inflation-induced changes in SVRI and SVCI were abolished at isoflurane concentrations of 2 MAC. We conclude that under the conditions of this study, 1 MAC isoflurane was shown to attenuate lung reflex-induced changes in SVRI and SVCI and that at higher isoflurane concentrations (2 MAC) these reflex-induced changes were not seen.

Hemodynamic status susceptible to slowing of heart rate during thermodilution cardiac output determination in anesthetized patients

To identify hemodynamic variables that might indicate susceptibility to slowing of heart rate (HR) and to mean arterial pressure (MAP) decrease caused by cold injectate during thermodilution (TD) cardiac output determination, we measured hemodynamic variables in 32 anesthetized patients undergoing major surgery. A total of 608 cardiac output determinations were evaluated for any relationship between the magnitude of HR decreases and basal hemodynamic variables. The magnitude of HR decrease was pronounced in low cardiac index (CI), low mean pulmonary artery pressure (MPAP), and high systemic vascular resistance index (SVRI). Although there was some decrease in MAP associated with cold injectate, neither changes in SVRI nor those in the other hemodynamic variables correlated with the decreases in MAP. These results suggest that decreased CI and MPAP associated with elevated SVRI may be more susceptible to slowing of HR during cardiac output determination by TD in anesthetized patients.

Relation of arterial blood lactate to oxygen delivery and hemodynamic variables in human shock states

A retrospective study of 50 patients with circulatory shock and serial hemodynamic and metabolic measurements was undertaken. From the patient records, values for first measured cardiac index (CI) (t = 1) and highest CI (t = 2) with concomitantly obtained hemodynamic and metabolic variables and with arterial blood lactate levels (ABL), measured within 1.5 hours of t = 1 and t = 2 were taken. Nineteen patients had nonseptic shock (NSS), and 31 had septic shock (SS). Mortality rates were equivalent. At both t = 1 and t = 2, CI and O2 delivery (DO2) were higher and systemic vascular resistance index (SVRI) was lower in SS than in NSS. Although increases in DO2 were significant and not different between the groups and initial ABL values were similar, ABL had declined 50% in NSS but had not changed in SS (p less than 0.0001). From the hemodynamic and metabolic variables investigated in NSS, changes in ABL only correlated with changes in arterial oxygen content (CaO2; r = -0.65; p less than 0.01). Changes in ABL did not correlate with changes in DO2 in both groups. In SS, changes in ABL best correlated with changes in SVRI (r = -0.54; p less than 0.01). Our data suggest that anaerobic metabolism, reflected by ABL, decreases in response to an increase in CaO2, CI, and thus DO2 in NSS but not in hyperdynamic SS. Anaerobic metabolism in the latter may relate to peripheral vasodilation, associated with peripheral "functional" shunting of blood transported oxygen, rather than to insufficient DO2.